Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Microbe-Host Interactions Training Program, Vanderbilt University, Nashville, Tennessee, USA.
J Infect Dis. 2021 Jul 15;224(2):360-365. doi: 10.1093/infdis/jiaa730.
Helicobacter pylori is the strongest risk factor for gastric adenocarcinoma. The H. pylori cancer-associated cag pathogenicity island (cag-PAI) encodes a type IV secretion system (T4SS), which translocates microbial DNA and activates TLR9; however, most cag-PAI+-infected persons do not develop cancer and cag-PAI-independent regulators of pathogenesis, including strain-specific adhesins, remain understudied. We defined the relationships between H. pylori HopQ adhesin allelic type, gastric injury, and TLR9 activation. Type I hopQ alleles were significantly associated with magnitude of injury, cag-T4SS function, and TLR9 activation. Genetic deletion of hopQ significantly decreased H. pylori-induced TLR9 activation, implicating this adhesin in H. pylori-mediated disease.
幽门螺杆菌是胃腺癌的最强危险因素。幽门螺杆菌相关的 cag 致病岛 (cag-PAI) 编码一种 IV 型分泌系统 (T4SS)，该系统可转移微生物 DNA 并激活 TLR9；然而，大多数感染 cag-PAI+的人不会发展为癌症，而 cag-PAI 独立的发病机制调节剂，包括菌株特异性黏附素，仍研究不足。我们定义了幽门螺杆菌 HopQ 黏附素等位基因类型、胃损伤和 TLR9 激活之间的关系。I 型 hopQ 等位基因与损伤程度、cag-T4SS 功能和 TLR9 激活显著相关。HopQ 的基因缺失显著降低了幽门螺杆菌诱导的 TLR9 激活，提示该黏附素参与了幽门螺杆菌介导的疾病。
